ABSTRACT
Inactivity accelerates muscle catabolism, mitochondrial dys-function, and oxidative stress accumulation and reduces aerobic capacity. This chapter aims to assess the role of exercise in enhancing mitochondrial function, biogenesis, dynamics, turnover, and quality control in aging muscle, as an area of research on bioenergetics and homeostasis, which has placed the mitochondria at the center of these processes. Mitochondrial dysfunction remains a common denominator of aging and it is considered to be part of the compensatory or antagonistic responses to the damage caused by cellular aging. In particular, the mitochondrial biogenesis signaling activated by the peroxisome proliferator-activated receptor gamma coactivator family of cotranscription factors is reduced with increasing age. Mitochondrial fusion and fission contribute to mitochondrial function by exchanging components such as membrane, proteins, and DNA. The chapter describes the pleiotropic effect of physical activity on multiple targets that have a role in preventing the decline of mitochondrial “quality,” which is implicated in the aging process of skeletal muscle.
